We have extended our earlier, preliminary findings on the role of brainstem GABA in the ethanol inhibition of baroreflex bradycardia in urethane-anesthetized rats. Ethanol, 1 g/kg i.v. or 25-200 nmol microinjected bilaterally into the medullary dorsal vagal complex (DVC), inhibited the reflex bradycardic response to iv. phenylephrine in control rats but not in rats pretreated with the GABA-depleting agent, 3-mercaptopropionate. Ethanol, 1 g/kg iv., did not influence the bradycardic response to electrical stimulation of the cervical vagus. Intra-DVC injection of muscimol caused a pressor response and inhibited baroreflex bradycardia. The pressor response was potentiated and a tachycardic response to muscimol emerged following intra-DVC injection of ethanol. Intra-DVC injections of baclofen also caused pressor and tachycardic effects and inhibited baroreflex bradycardia. Intra-DVC bicuculline selectively inhibited the effects of similarly administered muscimol, and attenuated the baroreflex inhibitory actions of ethanol. Intra-DVC 2-OH-saclofen selectively inhibited the effects of similarly injected baclofen and also attenuated the effect of ethanol on the baroreflex. Although 2-OH-saclofen did not influence the responses to muscimol, it inhibited the potentiation of the muscimol response by ethanol. It is concluded that ethanol inhibits baroreflex bradycardia by potentiating the similar actions of endogenous GABA in the DVC. Both GABA-A and GABA-B receptors appear to be involved in this effect.